Modifiable Risk Factors for Periodontitis and Diabetes
Author:
Publisher
Springer Science and Business Media LLC
Subject
Immunology and Microbiology (miscellaneous),Oral Surgery,Surgery
Link
http://link.springer.com/content/pdf/10.1007/s40496-016-0099-6.pdf
Reference150 articles.
1. Borgnakke WS. “Non-modifiable” risk factors for periodontitis and diabetes. Curr Oral Health Rep. 2016;3(3). doi: 10.1007/s40496-016-0098-7 . This report complements the current review as it describes the “non-modifiable” risk factors.
2. Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol. 2011;29(No Iss):415–45. doi: 10.1146/annurev-immunol-031210-101322 . This paper is the first to describe the low-grade, chronic, systemic inflammatory state that adipose tissue causes and coins this meta-inflammation coined “metaflammation.” This observation is based on the recent realization that adipose tissue functions as an organ that expresses pro-inflammatory biomarkers such as CRP and cytokines like TNF-α and interleukins. The authors use easy-to-understand figures to illustrate the obesity related inflammatory mechanisms due to the surplus of nutrients leading to excess adipocytes and subsequent to a chronic state of unresolved inflammation.
3. Janket SJ, Javaheri H, Ackerson LK, Ayilavarapu S, Meurman JH. Oral infections, metabolic inflammation, genetics, and cardiometabolic diseases. J Dent Res. 2015;94(9 Suppl):119S–27. doi: 10.1177/0022034515580795 .
4. Bartold PM, Van Dyke TE. Periodontitis: a host-mediated disruption of microbial homeostasis; unlearning learned concepts. Periodontol 2000. 2013;62(1):203–17. doi: 10.1111/j.1600-0757.2012.00450.x . This paper is a brilliant explanation by two giants in the field of periodontology of the development and sustainability of the viscious cycle leading to increased inflammation with increased periodontal tissue breakdown in a viscious cycle that is initiated by the microbial dysbiosis in dental plaque, but mediated by the host response rather than depending on particular periodontal microbes. While giving a nod to the initial importance of subgingival microflora in dental plaque, the authors argue that usual members of the subgingival microbiome in health (commensal) can show overgrowth as opportunistic pathogens, given the right constellation of facilitating host factors, that is, the host’s inflammatory responses are more responsible for the end result of periodontal breakdown than the identity of the periodontal microbes in the biofilm.
5. Lamont RJ, Hajishengallis G. Polymicrobial synergy and dysbiosis in inflammatory disease. Trends Mol Med. 2015;21(3):172–83. doi: 10.1016/j.molmed.2014.11.004 .
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